2. Cancer that arises in the epithelium, the tissue that lines the skin
and internal organs of the body, and has a malignant potential
aswell.
3. In general ovarian malignancy accounts for 25%
of gynaecological cancers.
Among ovarian tumors only 10% are malignant.
Malignant tumors are classified into;
◦ Epithelial tumors….that accounts for 90% of malignant
ovarian tumors.
◦ Non epithelial tumors…that accounts for 10% of malignant
ovarian tumors.
5. Not clerly known, however there are some factors
which are affiliated with Ca ovary.
◦ Incessant ovulation
◦ Age
◦ Geographic destribution
◦ Family history
◦ Infective agents
◦ Infertility treatment
◦ Pelvic irradiation
◦ Other factors such as asbestos, tale etc.
6. Direct spread.
◦ Neighbouring organs like fallopian tube, uterus, bladder
and pelvic peritonium.
Lymphatic spread.
◦ Via lymphatic channel to the diaphragm, omentum,
peritonial surfaces of small and large bowel , liver and
perital peritonium throughout the abdominal cavity.
◦ Also involves para-aortic and pelvic lymph nodes, and
may metastize to groin and cervical lymph nodes.
7. Blood metastasis.
◦ to the liver, lungs, bones and brain but occurs late in the
course of the disease.
8. Limited by two factors;
◦ Ovary is not an accessable organ.
◦ A premalignant stage of ovarian cance has not yet been
recognized.
Screening includes, bimanual pelvic examination,
ultrasonography and tumour markers.
9. Late presentation
Pain
Abdominal swelling
Abnormal uterine bleeding
Weight loss
Pressure effets
10. GPE
Pale and cachexic
Neck and groin examined for enlarged lymph
nodes and breast for primary or secondary
tumours
Legs should be examined for DVT
Abdominal examination
Abdomen may look distended and may have
prominent veins
On palpation malignant ovarian tumour appear
11. As a fixed ,tender,hard and irregular mass which
is more often bilateral
Pelvic examination
Firm,tender,irregular with restricted mobility due to
extension of tumour into surrrounding tissue
Rectal examination
to see the posterior extention of the disease.
13. Cytology.
◦ Fine needle aspiration done in clinically suspicious lymph
nodes in the groin and neck.
Tumor markers.
◦ CA-125 (<35 IU/mL)
Haematological investigations.
◦ Full blood count, urea , creatinine, electrolytes and liver
function tests.
14. The Federation Internationale de
Gynecologie et d'Obstetrique (FIGO) and
the American Joint Committee on Cancer
(AJCC) have designated staging.
15. limited to the ovaries.
◦ Stage IA: tumour limited to 1 ovary, the
capsule is intact, no tumour on ovarian
surface and no malignant cells in ascites or
peritoneal washings.
◦ Stage IB: tumour limited to both ovaries,
capsules intact, no tumour on ovarian surface
and no malignant cells in ascites or peritoneal
washings.
◦ Stage IC: tumour is limited to 1 or both
ovaries with any of the following: capsule
ruptured, tumour on ovarian surface,
malignant cells in ascites or peritoneal
washings.
16. tumors involving 1 or both ovaries with pelvic
extension and/or implants.
◦ Stage IIA: extension and/or implants on the
uterus and/or fallopian tubes. No malignant
cells in ascites or peritoneal washings.
◦ Stage IIB: extension to and/or implants on
other pelvic tissues. No malignant cells in
ascites or peritoneal washings.
◦ Stage IIC: Pelvic extension and/or implants
(stage IIA or stage IIB) with malignant cells in
ascites or peritoneal washings.
17. tumours involving 1 or both ovaries with microscopically
confirmed peritoneal implants outside the pelvis.
Superficial liver metastasis equals stage III.
◦ Stage IIIA: microscopic peritoneal metastasis beyond
pelvis (no macroscopic tumour).
◦ Stage IIIB: macroscopic peritoneal metastasis beyond
pelvis less than 2 cm in greatest dimension.
◦ Stage IIIC: peritoneal metastasis beyond pelvis greater
than 2 cm in greatest dimension and/or regional lymph
node metastasis.
18. • tumours involving 1 or both ovaries with distant
metastasis. Parenchymal liver metastasis
equals stage IV.
19. Dysgerminoma
Less than 1% of ovarian malignancies
Counterpart of testicular seminoma
Usually young patients (81% under age 30)
5% associated with gonadal dysgenesis/Swyer syndrome
androgen insensitivity or pseudohermaphroditism; rarely associated with
hypercalcemia
Metastasize to opposite ovary, retroperitoneal nodes, peritoneal cavity
Rarely transforms to yolk sac tumor
20.
Survival: 95%
treatment: surgery and chemotherapy (NOT
radiotherapy, although it is effective for seminoma)
Gross: 15% bilateral; solid, nodular, small to huge,
gray-pink(resembles cerebral cortex); hemorrhage
and necrosis common but less prominent than
other malignant tumors
Micro: nests of tumor cells separated by fibrous
stroma with T lymphocyteslarge vesicular cells with
well defined cell borders, cleared cytoplasm
containing glycogen, central nuclei;
21.
22.
Also called endodermal sinus tumor
May be derived from embryonal carcinoma
presentation
Usually children or young adults (median age 19 years) with
abdominal pain and rapidly growing mass,
increasing alpha fetoprotein (AFP) and alpha-1-antitrypsin serum levels;
negative hCG
Gross: mean 15 cm, smooth and glistening external surface, cystic cut surface
with hemorrhage and necrosis; often has benign teratoma component; rarly is
found in pelvis unattached to ovary
23.
24.
25.
Malignant tumor, whose tissue resembles embryonal or fetal tissue
Usually prepubertal or young women (mean 18 years)
Most recurrences within 2 years; presence of yolk sac component is best
predictor of recurrence in pediatric tumors
Treatment: surgery, multiagent chemotherapy; better prognosis if only mature
teratoma found after chemotherapy, although abnormal karyotype is maintained
in mature teratoma
Gross: bulky, solid or cystic with necrosis, hemorrhage
Micro: usually neurogenic elementsmesodermal elements common; some
tumors derived primarily of esophageal, liver and intestina
26.
27.
28. Also called Sertoli-stromal cell tumor; formerly
called androblastoma, arrhenoblastoma
Usually young women (mean age 25 years,
75%<age 30)
Rare, < 0.1% of ovarian neoplasms
80 % produce Androgens hence causing
masculinization
29.
30.
31. Also called dysgenetic gonadomaMixture of germ cell tumor and
sex-cord stromal tumo
Usually occurs in individuals with abnormal sexual development
and indeterminate gonads; usually gonadal dysgenesis with Y
chromosome
25% risk of neoplasia in these gonads
80% are phenotypic women, 20% are phenotypic men with
undescended testicles and female internal secondary organs
prognosis
Excellent prognosis if completely excised; almost never malignant
Gross: 36% bilateral, tumors usually small, may be microscopic
Micro: primitive germ cells and sex cord stromal cells surrounded
by ovarian-type stroma
32.
A Krukenberg tumor refers to a malignancy in the ovary that
metastasized from a primary site, classically the gastrointestinal
tract, although it can arise in other tissues such as the breast.
[1] Gastric adenocarcinoma, especially at the pylorus, is the most
common source.
[2] Krukenberg tumors are often (over 80%)[2] found in both
ovaries, consistent with its metastatic nature
Symptoms
Krukenberg tumors often come to the attention when they cause
abdominal or pelvic pain,
bloating,
ascites,
or pain during sexual intercourse.
33. Krukenberg tumors can occasionally provoke a reaction of the
ovarian stroma which leads to hormone production, that results in
vaginal bleeding,
a change in menstrual habits,
or hirsutism
or occasionally virilization as a main symptom.
Diagnosis
All these symptoms are non-specific and can also arise with a
range of problems other than cancer, and a diagnosis can only be
made following confirmatory investigations such as
computed tomography (CT) scans,
laparotomy
and/or a biopsy of the ovary.
34.
35.
36.
37. The treatment of ovarian cancers based on the
stage of the disease which is a reflection of the
extent or spread of the cancer to other parts of the
body.
It also depends on histologic cell type, and
the patient's age and overall condition.
There are basically three forms of treatment of
ovarian cancer:
◦ surgery
◦ Chemotherapy
◦ radiation treatment,
38. Standard treatment is surgery (staging and optimal
debulking) followed by adjuvant chemotherapy in most
cases. Even if optimal surgery is not possible, removing
as much tumor as possible will provide significant
palliation of symptoms.
Borderline lesions may be treated with conservative
surgery
39. Advanced epithelial ovarian cancer is very sensitive to
chemotherapy with responses in the range of 70-80% to
first-line chemotherapy. The majority, however, relapse
and ultimately die of chemotherapy-resistant disease.
Second-line chemotherapy to date is disappointing in all
forms of epithelial ovarian cancer with virtually no
chance of successful second-line treatment following
failure of initial regime.
40.
41.
42. Stage of cancer Post op. therapy
Stage 1a (intact capsule
grade 1-2)
Stage 2b-3a
Advanced/recurrent
disease
No furter treatment
Chemotherapy or whole
abdominal radiotherapy
Palliative:chemotherapy,
radiotherapy, harmone
therapy, immunotherapy
43. Prolongs remission and survival
Also used for palliative treatment in advanced n
recurrent disease
Administered in all cases beyond stage Ia
Earlier single agents were used, nowadays combination
therapy is favoured
45. Combination therapy is most beneficial.
Drugs are given at 3 weeks intervals
Intraperitoneal chemotherapy is also done but is very
effective.
46. The initial treatment of ovarian cancer is called first line
therapy.
First-line chemotherapy for ovarian cancer typically
consists of two drugs given together. The combination
=paclitaxel + platinum drug—either carboplatin or
cisplatin.
47. Now, has a very small role since platinum based
protocols and paclitaxel have improved the median
survival.
-However it can be used as a palliative treatment for
metastatic bone or brain lesions or of localized
recurrence to alleviate the pain.
48. CA-125
Second look surgery in the form of laprotomy or
laproscopy.
49. Overall 5-year survival in ovarian epithelial carcinoma is low
because of the preponderance of late-stage disease at diagnosis.
◦ Stage I and II: 80-100%
◦ Stage III: 15-20%
◦ Stage IV: 5%
Patients under 50 in all stages have considerably better 5-year
survival than older patients (40% compared to 15%)
50. Diet: a high-fat diet may play a role in the
aetiology of ovarian cancer.
Oral contraceptives appear to reduce the risk of
ovarian cancer for up to 10 years following
cessation of use. This protective effect appears
to apply to patients with BRCA mutations as
well.
Patients who have used fertility drugs should be
counselled as to their possible increase in risk of
ovarian cancer.